1. Field of the Invention
The present invention relates to the monitoring of haemodynamic parameters. More particularly, the present invention provides an apparatus and method for monitoring patients' osmotic or oncotic pressure in situ.
2. Background of the Invention
Apparatus for measuring hydrostatic pressure in situ is well known. A catheter is commonly inserted into a central vein or into a pulmonary artery for this purpose.
However, fluid exchanges occurring between the blood stream and body tissues which produce conditions such as pulmonary edema are governed by osmotic pressure effects, particularly colloid osmotic pressure (COP), as well as hydrostatic pressure. Monitoring these exchanges in critically-ill patients and high-risk surgical patients is particularly important, but in these cases it is also very important to minimize the effect of such monitoring on the patient's physiological condition. For example, COP monitoring can be valuable in the management of shock, myocardial infarction, serious burns, malnutrition, and hepatic or renal failure cases, but the need to minimize the risk to these patients induced by such monitoring is self-evident.
Intravascular osmotic pressure can be intermittently determined by measuring molar freezing point depression or by measuring the protein content of a blood sample. However, either measurement involves time delays and repeated blood withdrawals that make such a method cumbersome and ill-suited to monitoring critically ill patients. Furthermore, measurement of freezing point depression indicates only total osmotic pressure, and the determination of COP by measurement of the protein content of blood is very sensitive to laboratory errors in protein measurement. The Landis-Pappenheimer formula on which the latter approach is based is a species-specific exponetial function of blood protein for a given body temperature: EQU COP=xC+yC.sup.2 +zC.sup.3
where:
C=total protein (grams/dl)
x, y, z=temperature-variable constants Further discussion of this method can be found in the American Physiological Society's Handbook of Physiology (Washington, D.C., 1963) Circulation Vol. 2, pp 961-1034.
Continuous extracorporeal monitoring of COP can be achieved by shunting the bloodstream through external disc or needle osmomitors. These devices are described by Weil et al in U.S. Pat. No. 4,028,931 and by Kakuichi et al in U.S. Pat. No. 4,245,495, respectively. However, the shunting of the bloodstream through external devices is cumbersome at best. For critically-ill patients this shunting often represents an unacceptable risk, particularly when blood pressure or blood volume is low for any reason.
Additionally, it has been suggested that pulmonary edema can be produced by local changes in COP that are not readily observable elsewhere in the patients' system. Thus, the location at which COP is measured has a potentially significant effect of the usefulness of the measurement. This further complicates methods of COP determination requiring either shunting of the bloodstream or repeated blood withdrawal.
An experimental single-lumen device for short-term intravascular monitoring of COP in heparinized animals was disclosed by Henson et al, Am. J. Physiol. pp H726-H729 (1983). The device consists of a single catheter lumen terminated by a closed-end semipermeable tube and by a pressure sensor, respectively. This device is not suitable for use in human subjects, nor is it suited for use in continuous monitoring of COP in situ.